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Mechanistic investigations revealed that PTX resistance was primarily mediated by EV-derived VDAC1 through the AMPK/mTOR pathway, which involved activation of general autophagy and mitophagy

Cells treated with DMSO, 10 nM dBET6, 100 pM IBG3, 2 M dHTC2, or 10 M dHTC3 (16 h)

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While it may be argued that our study used relatively small group sizes, the results were significant and reproducible, consistent with the large effect sizes and low variability of our experimental paradigms

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Furthermore, comparative investigations help support organized research methodologies and repeatable laboratory workflows